Research Paper Volume 16, Issue 8 pp 7174—7187
Promoter hypomethylated PDZK1 acts as a tumorigenic gene in glioma by interacting with AKT1
- 1 Clinical Laboratory Medicine Center, The First Affiliated Hospital of University of South China, Hengyang 421001, Hunan, P.R. China
- 2 Cancer Research Institute, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, P.R. China
Received: November 15, 2023 Accepted: March 25, 2024 Published: April 25, 2024
https://doi.org/10.18632/aging.205750How to Cite
Copyright: © 2024 Ren et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Glioma is the most frequently diagnosed primary brain tumor and typically has a poor prognosis because of malignant proliferation and invasion. It is urgent to elucidate the mechanisms driving glioma tumorigenesis and develop novel treatments to address this deadly disease. Here, we first revealed that PDZK1 is expressed at high levels in gliomas. Promoter hypomethylation may cause high expression of PDZK1 in glioma. Knockdown of PDZK1 inhibits glioma cell proliferation and invasion in vitro. Mechanistically, further investigations revealed that the loss of PDZK1 expression by siRNA inhibited the activation of the AKT/mTOR signaling pathway, leading to cell cycle arrest and apoptosis. Clinically, high expression of PDZK1 predicts a poorer prognosis for glioma patients than low expression of PDZK1. Overall, our study revealed that PDZK1 acts as a novel oncogene in glioma by binding to AKT1 and maintaining the activation of the AKT/mTOR signaling pathway. Thus, PDZK1 may be a potential therapeutic target for glioma.